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Dinasil as a toxin binder

Dinasil is a product that is formulated to bind toxins produced by molds (mycotoxins) in such a way that it will not be absorbed by the animal.

What does Dinasil contain?

Dinasil contains Aluminum silicate.

How does Dinasil works?

Dinasil binds mycotoxin inside the animals digestive system allowing the mycotoxin to pass through without causing any harm.

Does Aluminum Silicates bind other minerals?

Based on studies conducted at the University of Georgia there is no nutrient binding that occurs in the animal feeds. If however binding does occur the potential is of very low magnitude and would result in only minor consequence on the animals perfor­mance.

Why do I need to include mold inhibitor in the feeds?

It is stated that molds can potentially grow starting from the field up to the house of the animals. Once the mold grows it begins to produce mycotoxins which causes many harm to the ani­mals. A toxin binder is the only means of getting rid of these harmful toxins after they are produced in the feed.

Is it still necessary to put a toxin binder if mold inhibitor is already mixed in the feeds?

Yes. A toxin binder is specifically used to bind mycotoxins produced by molds, while a mold inhibitor stops mold reproduc­tion.

When molds are present, toxin is consequently produced there­fore, a toxin binder is necessary.

A very effective preparation for protection against molds and toxin is Dinasil PLUS which is a combination of a mold in­hibitor and a toxin binder. This will better protect the essen­tial nutrients in feeds as well as your animals. Mycotoxicosis is no more a worry.

How much Dinasil and Dinasil PLUS will I place in a ton of feed?

Dinasil is added at a rate of 1 kg per ton of finished feed.

Dinasil PLUS is added at 1 ‑ 2 kg in every ton of feed.

EFFECTS OF MYCOTOXICOSIS ON POULTRY

Some are carcinogenic and many are synergetic with pathogenic or disease conditions. For example there a corroborated evidence to sustain the impairment of immunity response of affected animals (Charts 2 & 3). There is also documented synergism with coccidiosis, salmonella, (Chart 4) crop mycosis and nutritional deficiencies (Chart 5) (Poultry Science 53;721‑725, 1974 immunal suppression in chickens by aflatoxins, J.P. Faxton, H.P. Tung and P.B. Hamilton). "The relative sizes of both the bursa of fabricious and thymus were reduced by dietary aflatoxin. The bursa decreased by approximately 1/4 at the higher doses of aflatoxins while the thymus regressed to about 1/2 of normal size".

The study indicates that dietary aflatoxin is a potent immuno-suppressant in the young chicken and that the extent of suppression of that response is related to the dose of aflatoxin as well as the duration of the treatment. Poultry Science 54; 1693‑1696, 1975 interaction of T2 toxin with salmonella infections of chickens. Boon Bungearn Boonchuvit, P.B. Hamilton and H.R. Burmeister "The interaction demonstrated between T2 toxin and para typhoid infections which manifest themselves as increased mortality, has important implications for the poultry industry" (Chart 4).

The severity of mycotoxicosis will probably vary widely and any of the following parameters will have a marked influence . Things such as level in the substrate, condition of litter, age of livestock, ex of livestock, genetic compliment, environment, temperature, humidity, the state of nutrition, the state of production and presence of other diseases (Chart 6). One well known kind of mycotoxin is called aflatoxin. Aflatoxicosis is the related problem to the aflatoxin generating types of molds. Aflatoxins have received more attention in the last few years, this is mainly due to feed or litter infection in poultry. It is known to be responsible for poor feed conversion and loss of egg production. Aflatoxins have the following etiology.

There are several types ‑ B1 ‑ the most important in poultry. B2, G1, G2, M1 and M2 which are related to dairy cattle and others(8). Aflatoxins are produced by aspergillus flavus and Aspergillus Parasiticus and some species of penicillia. The substrate can be found in corn, barley, millet, peanut peas, rice, sorghum, wheat, coastal hay and oats. Smith and Hamilton Poultry Science 49; 207‑215, did a study which centered around the percent positive feed ingredients for aflatoxin taken from several sources. The study indicated an ascending level of positive incidence with aflatoxin content going from 0%, soybean meal 5%, corn 30%, feed from the mill 52%, and feed from the trough at 91% positive rate. This is quite important. These troughs had a high concentration of positive results when tested for aflatoxins.

(8) HAMILTON ET AL

Mold problems are enhanced throughout the feed chain process starting with harvest, the problems related to excessive handling, inadequate drying, holding too long before drying without ventilating, improper storage and cleaning, moisture buildup in bins from leakage, from lack of aeration, insect damage in storage, poor sanitation, and poor clean up of bins and feeders. There are many things that are related to mold contaminated feed and its effects on livestock performance. Some of the most important ones can be summarized as depressed weight gain and reduced feed efficiency. For layers we find decreased feed intake and drop in egg production, on broilers there is decreased carcass quality as well.

North Carolina State University conducted a study which shows that the amount of #1 quality carcasses decreased from 59.6% To 28.8% When comparing a group of broilers which had been treated with anti‑molding solutions (See Chart 8) the external symptomatology of mycotoxicosis problems can be summarized as follows: in the poultry industry you will find increased morbidity, increased mortality, a higher percentage of deformed legs. In the processing plant increased bruising (See Chart 9) both inside and outside of the skin layers, Drs. Tung, Smith, and Hamilton corroborate the effects of aflatoxicosis on bruising in the chicken in their paper #3248 of the journal series of the North Carolina State University Agricultural Experiment Station in Raleigh, North Carolina, in which they state "the finding that aflatoxin can make chickens more susceptible to bruising has significance to the poultry industry since bruising results in condemnation losses of several million broilers every year. The introduction of susceptibility to bruising by doses of aflatoxin too small to inhibit growth and the occurrence of this condition within 48 hours after the aflatoxin is incorporated into the diet indicate the insidiousness of aflatoxicosis and the difficulty of diagnosing and controlling it."

Intestinal fragility during ochratoxicosis and aflatoxicosis has been demonstrated by Drs. Warren and Hamilton in their paper 6132 of the journal series of the North Carolina State University Agricultural Experiment Station in Raleigh, North Carolina. Ochratoxins were found to debilitate the intestinal wall. Post mortem lesions associated with mycotoxicosis include but are not limited to the following: pale yellow fatty livers and distended gall bladders, congested kidneys usually enlarged, hemorrhaging of muscles and viscera, regressed bursa of fabricious and thymus, enlarged spleen and pancreas, hydropericardium and acetis pale bone marrow.

In problems related to aflatoxicosis the target organ is the liver and the most sensitive metabolic systems are protein synthesis, lipid synthesis and lipid transport. Increased lipid content of the liver has been substantiated and has been observed to increase from 30% to over 60% in as many as 10 parts per million content of aflatoxins. (See Chart 10). Bone strength of livestock also is affected. Drs. Hoff, Doerr, Hamilton, Hamann, Peterson and Ziegler in their paper titled "Evaluation of bone strength during aflatoxicosis and ochratoxicosis", conclude that aflatoxin and ochratoxin have debilitating effects on bone properties. The breaking strength, of the bones, was decreased and the flexibility of the bones was increased. Gizzard erosion, crop mycosis, oral lesions caused by ingestion of dietary fusariotoxin have been documented by Drs. Wyatt, Weekes, Hamilton and Vermyster (See Applied Microbiology August 1972 pages 251‑257). Also documented has been the interference with pigmentation or carotenoid metabolism during ochratoxicosis in young broiler chickens.

EFFECTS ON DAIRY CATTLE AND PIGS

In addition to the problems related to poultry, mycotoxicosis is a dangerous entity for other livestock farmers. It has been substantiated that milk production by dairy cattle can be reduced drastically by mycotoxicosis. This phenomenon may not be due directly to the mycotoxicosis effect but the result of the cattle consuming less feed normally within 12 hours of consumption of aflatoxin, for example, with the resulting decreased milk production 2 days later.

The following is a summary of the symptoms of aflatoxicosis in dairy cows which have been observed in nine different studies by Mertens, D. R., 1979. "Biological effects of mycotoxins upon rumen function and lactating dairy cows. In; " Interactions of mycotoxins in animal production" PP. 118‑136. National Academy of Science U.S.A., Washington, D.C.:

7) Elevated blood levels of cholesterol, bilirubin, and the enzymes aspartate and

aminotransferase. Lactic dehydrogenase and alkaline phosphates.

8) Edema of the abdominal cavity.

We know many of these findings are not necessarily specific for aflatoxicosis therefore making a diagnosis becomes that much more difficult. Added to this problem is the fact that with ruminants it is very difficult to say whether the toxin in question is causing a malfunction of the rumen or a systematic toxicity.

This is particularly true with certain types of mycotoxins which can have a very strong anti‑microbial activity. We know from both "in vitro" and "in vivo" studies that aflatoxin impairs rumen function by decreasing cellulolysis, production of volatile fatty acids and ammonia and by altering the proportions of the volatile fatty acids produced. One very important area to look at with dairy cattle is the possibility of toxic residues occurring in the products consumed by humans. This is particularly important with lactating cows which may excrete mycotoxins or their metabolites in milk. Since milk is a major component in the diet of babies and children, and as the young of any given species are much more susceptible to this problem than adults this becomes a paramount problem for the livestock farmer and the marketing sectors to deal with. Mr. Armbrecht et al. Reports his finding upon giving sows feed containing 100 parts per billion of aflatoxin and found that from these 1.5 parts per billion were found in the milk and 8 parts per billion were located in the livers of the nursing pigs.

In dairy cattle there was a linear relationship between intake and excretion in milk which correlates to 1% of the intake being excreted as a toxic metabolite of the incoming aflatoxin.

Mycotoxins also cause a severe problem in the swine industry. F‑2 toxin (Zearalenone) for example has been known to cause a number of problems: among these infertility, false heat, hyperestrogenic activity and in some very sensitive animals, like pigs, this F‑2 toxin can produce also swollen edematous vulva and vaginal prolapse in addition an enlarged uterus and atrophy of the ovaries can be observed. Ovulation is hindered by the oocytes that can die in the graafian follicle. Because of the fact that the uterine glands in the mucosa of the uterus degenerate, ovulation and fertilization become difficult to maintain. You will also observe in male pigs atrophy of the testes and the development of the mammary glands evident.

From a nutritional perspective we know that molds reduce the value of foods. Several nutrients are affected by molds. For example energy contents and vitamins A, D, E and K, minerals and protein contents are all affected by mold infestation. From Bartow et al., 1982 we learn some of the devastating effects of molds on corn quality. Good quality corn was compared with moldy corn and was supplemented with soybean oil. Measurements were taken to determine weight gain and feed to gain ratios. The good corn with a 1% soybean oil level had a weight gain of 767 gr. And a feed to gain ratio of 1.79. Moldy corn with the same level of soybean oil only had a weight gain of 713 gr. With a feed to gain ratio of 1.96. The soybean oil level was increased from 1 to 2 to 4% in the moldy corn and only at the last level was the weight and gain brought back to the original level of the good corn and the feed to gain ratio in line with the good corn.

The implications of this are evident. (See Chart 13). There is a significantly decreased amount of energy available to animals when molds are present in feedstuffs. In the same study by Bartov, several effects of mold development on a few nutritional components of corn were measured. Again good corn was compared to moldy corn and such things as vitamin E carotene level and crude protein were measured. In the case of Vitamin E, the moldy corn had 6.8% less Vitamin E, 25.8 less milligram per kilogram of Carotene. There was no change observed in the crude protein. In the same study total fat was shown to be reduced from good corn to moldy corn by as much as 36.8%. The fatty acid composition was affected mostly in the 16;0 chain of 11.3 to 9.1% for a total decrease of 19.5%. (See Chart 14).

EFFECTS OF MOISTURE

Moisture is one of the most important parameters for mold reproduction. The effects of high moisture conditions in the nutritional quality of corn have also been quantified. A study was conducted to measure the difference between 12%, 15% and 18% moisture corn. Measurements were taken of gross energy crude protein fat, calcium and phosphorous. The gross energy for the 12% corn was 3483 calories, 3345 for the 15% corn and 3287 for the 18% corn. Crude protein went down 8.33% on the 12% to 7.83 on the 15% corn and then up to 11.2% on the 18% corn. Fat went from 3.77% on the 12% corn to 2.7% on the 15% corn and 1.92% on the 18% corn. Calcium went from .03 to .008 to .006 respectively and phosphorous from .18 to .03 to .03. (See Chart 15). Furthermore, moisture conditions of corn on the performance of 3 week old broiler chicks were measured, Veltman et. al., 1984.

Different percentage moisture corns were compared. In this particular case 12, 15 and 18% corn moisture was used. Body weights and feed gain were measured. For the 12% moisture the body weight came at 470 gr. and the feed to gain ratio at 1.68, 15% had 463 gr. and 1.9 respectively, and 18% had 458 and 1.91 respectively. (See Chart 16).

We summarize that the outcome of mold infestation is that it will affect all of the nutritional characteristics of feedstuffs therefore making it very expensive for livestock growers to have the problem.

Once you have the problem the only possible action is to discontinue use of the contaminated feed or use a proven aflatoxin binder in the feed. This in itself is a very costly proposition. Also increasing the protein, fat, vitamin and electrolyte level of the diet may be of help. Fat level can be increased by 1 to 2%; the trace minerals can also be increased as well as the vitamin mix. As always with any disease problem the best cure is prevention and preventing mold growth requires a judicious management practice.

PREVENTION PROGRAM

We at Diversified Nutri-Agri Technologies recommend a comprehensive mold prevention program. This comprehensive mold prevention program begins with the quality control of the raw materials all the way through the feed mill, delivery systems, storage bins at the farm, feed troughs and litter conditions in the poultry and livestock houses. Together with this we believe that the use of a mold inhibitor is of great help in reducing the risk of mold infestation. We at Diversified Nutri-Agri Technologies do not believe that the use of a mold inhibitor by itself is the panacea or the magic wand that will solve the problems associated with molds.

Preventing the problems of mycotoxicosis begins with a good quality control program and the purchase of good quality corn. An ingredient assay program is a must. Contaminated feed ingredients must be rejected from a technical perspective, or "averaged" and treated with toxin binders if in practice the ingredients must be used. Feed storage time must be reduced to a minimum. Feed bins and handling equipment must be kept clean, the equipment must be periodically emptied and cleaned out and then disinfected with for example a 10% clorox solution. Steps must be taken to assure that low moisture ingredients are used and that they are not allowed to become damp.

Dinasil-Plus® MODE OF ACTION

The following is an explanation of how Dinasil-Plus® worksas an effective adsorbent & fungicide

I. The Adsorption Component of Dinasil-Plus precludes absorption of aflatoxins through the intestinal wall membrane

Scientific research findings indicate that Dinasil®* is a high affinity sorbent for aflatoxin and forms a stable complex metallic bond with this mycotoxin. The resulting bond makes it difficult for the adsorbed aflatoxin to pass through the intestinal wall into the animals organism. Less than 2-4 % do greatly reducing the risk of aflatoxicosis. Results suggest that Dinasil®* can significantly decrease the toxicity of aflatoxin via sequestration in the GI tract and reduced bio availability in vivo.

Further work is currently in progress to elucidate the molecular mechanism and specificity of this action and to develop optimal sorbents for the biosequestration of aflatoxins and other important mycotoxins in livestock and poultry. In conclusion, a combination of effective, field‑practical methods to detect and detoxify these hazardous substance may greatly facilitate an integrated approach to their preventive management of mycotoxins.

II. The Mold Inhibiting Component of Dinasil-Plus

Dinasil-Plus® not only effectively adsorbs aflatoxins in the intestine but it also interferes with mold cell wall respiration thereby disrupting active membrane exchange mechanisms and adversely affecting tho mold organism in at least four ways to wit:

1. Allowing toxic substances to enter the through the cell wall

2. Not allowing needed substances to enter through the cell wall

3. Preventing toxic substances from permeating through the cell wall

4. Allowing beneficial substances to escape through the cell wall.

In addition the rapid acidification within the cytoplasm interferes with RNA functions thereby interfering with protein synthesis processes

One hundred eight (108) piglets were randomly distributed to three treatments with 36 piglets per treatment divided into 12 piglets per pen following the randomized block design. Piglets in treatment I were fed with control diet while those in treatment II and III were fed with mycotoxin binders supplementation (Dinasil) and commercial mb, respectively. Piglets were fed for forty (40) days. Males (M) and females (F) were equally distributed for each pen 6 Males: 6 Females.

The results of the study showed that the final weight gain of the pig had no significant differences among treatments, however, the final weight of the pig fed with Dinasil mb supplementation was highest regardless of the lowest initial weight of the pigs. Therefore significant differences (P<0.05) were observed in change in weight and in average daily gain in treatment I vs. the control but not with commercial mb (treatment III). The results of the study revealed that the piglets fed with Dinasil mb supplementation was the best converter of feed (1.84) as compared to the control (1.99) and commercial mb (2.00).

The cost of feed per kg gain was highest in diet with commercial (mb) supplementation (P19.48) which was reflected with the highest feed consumption followed by the control, T1 (P19.01) and T2 Dinasil mb (P17.92). Therefore with Dinasil (mb), supplementation there is a saving of (P1.09) per kg gain. The results indicate that the supplementation of the diet with Dinasil (mb) enhanced the profitability of swine raisers. This was brought about by the significant overall growth performance of the piglets fed hog starter diet with Dinasil mb supplementation.